Alzheimer’s Disease: Polypeptide Hypothesis
*Corresponding Author: John Cheung-yuen Chan, An Individual Author, Kensington NSW 1465, Australia, Email: chantrading@bigpond.comReceived Date: Jul 29, 2022 / Published Date: Sep 01, 2022
Citation: Chan JC (2022) Alzheimer’s Disease: Polypeptide Hypothesis. J Alzheimers Dis Parkinsonism 12:549.DOI: 10.4172/2161-0460.1000549
Copyright: © 2022 Chan JC. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
| Peer-reviewed Full Article 
Abstract
Alzheimer's Disease (AD) has no cure yet and will approach 150 million cases in 2050. Pathologically, it is characterized by intracellular neurofibrillary tangles, extracellular amyloidal protein and brain atrophy.
The proposed AD hypothesis follows: Use four hypotheses, step by step, to conclude this AD hypothesis: “Most neurodegenerations are caused by abnormal protein (polypeptides) synthesis in neuronal cells.” The rationale is the following: Memory activities require energy and protein synthesis. The Reactive Oxygen Species (ROS) could damage neuronal DNA during protein synthesis, and the most DNA damage site is the "enhancer region," which controls the activity of genes when DNA is mistakenly repaired. The mistakenly repaired DNA strand served as a template for future mRNA, which could synthesize abnormal proteins, such as amyloids or tau. The mitochondria gradually lose their functions by reducing the energy production of the ATP and creating more ROS. The "mitochondria dysfunction" increase as human age. This AD hypothesis links the mitochondria dysfunction hypothesis and the amyloid cascade hypothesis.
The Late-onset AD (LOAD) progression timeline is not linear. Instead, it is an exponential degeneration, implying the LOAD progression is a positive feedback loop (vicious cycle). A good lifestyle may slow down disease progression.
